AJP - Renal Physiology, Vol 253, Issue 4 712-F718, Copyright © 1987 by American Physiological Society

ARTICLES

Calcium and vitamin D metabolism in spontaneously hypertensive rats

C. H. Hsu, C. S. Yang, S. R. Patel and M. G. Stevens
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109.

We have studied the effect of dietary vitamin D restriction on serum levels of vitamin D metabolites in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Both WKY and SHR were fed a vitamin D-deficient or a vitamin D-supplemented diet beginning at 4 wk of age. In vitamin D-supplemented animals, the serum 1,25-dihydroxycholecalciferol [1,25(OH)2D3] concentration of WKY (55.4 +/- 6.6 pg/ml, n = 5) was similar to the level of SHR (46.3 +/- 5.9 pg/ml, n = 5). Plasma calcium concentration was not different between WKY and SHR. In animals fed a vitamin D-deficient diet, the serum concentration of 1,25-(OH)2D3 of SHR (23.0 +/- 1.3 pg/ml, n = 5) was significantly lower than that of WKY (67.6 +/- 4.6 pg/ml, n = 5, P less than 0.01). Plasma 25-hydroxycholecalciferol level was markedly decreased in both WKY (3.6 +/- 0.5 ng/ml, n = 7) and SHR (2.8 +/- 0.4 ng/ml). The SHR, but not the WKY, developed hypocalcemia (WKY, 9.68 mg/dl; SHR, 6.70 mg/dl). Despite hypocalcemia, fasting urinary Ca2+ excretion of SHR exceeded that of WKY. We conclude that the lower 1,25(OH)2D3 level in SHR fed a vitamin D-deficient diet may be due to a defect in the synthesis of 1,25(OH)2D3. The low level of 1,25(OH)2D3 is associated with renal wasting of calcium and hypocalcemia in SHR.

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